.Chapter 8 – Hormones and Social Behavior
Behavioral changes occur in the development of addictive disorders similar to those that occur in social bonding. The neuropeptides oxytocin is critical in the partner-preference decision and addictive disorders. Oxytocin is a hormone that is associated with complex social behaviors such as parental care, social bonds, and sexual behaviors. Oxytocin is a small neuropeptide created in the hypothalamus and released into the bloodstream through the posterior pituitary gland. It acts centrally and peripherally. Studies have concluded the involvement of OT in the development and maintenance of attachment and affiliative behaviors. While OT is associated with social behaviors it is also involved in addictive disorders.
Oxytocin plays a central role in the regulation of affilitative behaviors. It is produced in the parvocellular neurons of the PVN, which extends to the hippocampus, amygdala, hypothalamus which are in the limbic system. It also extends to the locus coeruleus and the nucleus of the tractus solitaries which are in the mid-brain and hindbrain nuclei. In recent studies, Oxytocin has been recognized for its effects on a wide range of social behaviors such as social motivation and approach behavior. In humans, several experimental studies have found positive effects of intra-nasally administered OT on a large amount of social behaviors, including generosity, trust, face recognition, emotional perception, and more pair-bonding related phenotypes such as communication and behavior in conflicts between couples (Hasse Walum et al, 2012). The study performed by Walum et al had a result of significant associations in several of the samples used between variation in Oxytocin and phenotypes that were related to pair-bonding behavior in both women and girls provided conclusive evidence that Oxytocin can be of relevance for humans. This study supported the idea that oxytocin can enhance social bondings when intranasally administered.
In a study conducted by Theodoridou et al, the effects of one intranasal does of oxytocin were tested to determine judgements of facial trustworthiness and attractiveness. The study concluded that the administration of oxytocin had a positive effect of social behaviors such as trustworthiness and attractiveness ratings on both males and females. The study provided evidence that supports the general role of oxytocin and positive trait judgments. The neural structure involved in this process is assumed that first the amygdala activity is dampened which leads to the inhibition of defensive behaviors which enhances affilitative behaviors. This is caused by oxytocin.
Studies have shown that when oxytocin is manipulated to babies after childbirth, it can have a long-lasting effect on the expression of social and sociosexual behavior and the different instruments that regulate these behaviors. It has been shown in prairie voles that when oxytocin is manipulated, it increases the number of oxytocin neurons in the paraventricular nucleus of the hypothalamus. Also, oxytocin manipulation can change estrogen receptors both the MPOA and the VMN areas in the brain. These results portray that when oxytocin is manipulated, it can change the organization of the brain and the neural reaction to social stimuli. The study conducted by Kramer et al, 2006 was to see if oxytocin does affect the central nervous system and promote social behavior.
While oxytocin has shown positive features in behaviors, it can also be negative. Oxytocin is involved in the development and regulation of social behaviors such as attachment and addiction. Oxytocin, like other neuropeptides, affects central nervous system processes that are related to opiate ethanol and cocaine addiction. Oxytocin is created in the brain and then released at the posterior pituitary and the central nervous system. It has become more observable that neurohypophyseal neuropeptides play a vital part in drug addiction progression. In oxytocin, adaptive components of drug addiction are affected primarily: the neuropeptide inhibits the development of tolerance to, and physical dependence on, morphine and reduces the self-administration of another frequently abused opiate drug, heroin. Development of ethanol tolerance and that of cocaine sensitization also is inhibited by OXT treatment (Kovacs, Sarnyai, and Szabo, 1998). In the study conducted by Mary R. Lee et al, OT was intranasally administered to cocaine dependent subjects and the effects of oxytocin in cocaine addicted subjects were investigated. The study proved that the administering of OT increased the baseline desire to use and response portrayed excitement in the subjects with drug cues. The study’s results were from a single administration of OT to each subject and it portrayed that OT may enhance the urge to use.
The following studies have concluded the involvement of OT in the development and maintenance of attachment and affiliative behaviors as well as drug addiction. Oxytocin is a feel good hormone and promotes feelings of loved, which some get from the use of drugs. The common characteristic of social bonding and drugs is that from oxytocin the feeling of pleasure is similar.
Chapter 9 Hormones and Homeostasis
Homeostasis refers to an organism or an environments capability to return to stability after a change. The digestive system is restored from nutrients that come from food when necessary. The body depends on the breakdown and absorption of nutrients. Generally, an abundance of mechanical, chemical, and enzymatic processes help maintain digestive system homeostasis. Some hormones can enhance the process of digestion and absorption of nutrients and are vital for the maintenance of homeostasis. Hormones regulate the system for feeding behaviors and digestion. To help keep the body balanced, digestive hormones support the body so everything moves smoothly within the gastrointestinal tract. In some cases if the body and its hormones cannot function properly, it can result in human disease.
Glucose is a carbohydrate, and is an important simple sugar in the human metabolism. Glucose homeostasis is the balance of insulin and glucagon to maintain blood glucose. Humans use glucose for the production of several important elements, such as starch. Starches are the main food basis of glucose. In humans, starch α-glucogenic digestion entails a group of six enzymes. Two are soluble salivary and pancreatic amylases, two are associated with the small intestinal brush border membrane protein sucrase-isomaltase complex, and the last two with the intestinal brush border membrane protein maltase-glucoamylase complex in humans (Nichols, et al 2009).
There are four phases of glucose homeostasis. The first is the nutritional status, then the origin of blood glucose, followed by tissue using glucose, and finally major fuel for the brain. Glucagon is a hormone produced in the alpha cells of the pancreas. When blood glucose gets too low, the alpha cells release glucagon, which causes glycogen to be transformed into glucose (Petersen, K. F., 2004). When levels of glucose get too high, insulin is released from beta cells in the pancreas and converts glucose back to glycogen for homeostasis. Insulin and glycogen help regulate the body and avoid disease such as diabetes. When hormones are not regulated it caused the body become unstable and result in negative effects. Insulin resistance appears to be the best predictor of the development of diabetes.
Obesity is a medical condition commonly seen all over the world. It is a complex disorder that is caused by excessive fat. The hormone Ghrelin, a peptide that is mostly produced in the stomach, plays an essential role in the regulation of homeostasis within the body. Ghrelin regulates food intake, energy metabolism, and storage, as well as in insulin sensitivity. Ghrelin is expressed in hypothalamus as well as many other central and peripheral tissues. Ghrelin helps control food intake and energy metabolism at central levels as well as at peripheral levels. In humans, circulating levels of ghrelin are small in obesity (Pacifico et al, 2009).
Ghrelin administration stimulates GH secretion but also leads to weight gain. This is caused by an increase in food intake and reducing fat utilization. In a study conducted by Tschöp et al, ghrelin is shown to downregulate in human obesity. Downregulation in human obesity may be a result of higher than usual levels of insulin or leptin. This is possible when fasting plasma ghrelin levels are negatively correlated with fasting plasma levels of insulin and leptin (Tschöp et al, 2001). In the study, they further examined that the decreased secretion of ghrelin could be responsible for reduced levels of circulating GH in obese individuals. The study proposed that the reduced plasma ghrelin concentrations perceived in obesity represent a physiological adaptation to the positive energy balance associated with obesity.
Leptin is another hormone involved in the homeostasis of the human body and if not regulated can cause obesity. Leptin is secreted by adipose tissue that works in the central nervous system as negative feedback signal. This regulates appetite and metabolism. Extremely obese individuals have high leptin levels. This suggests that they are resistant to its metabolic effects, thus resulting in the obesity. In a study conducted by JH Lee, DR Reed, and RA Price, they found that leptin resistance appears to be common in their extremely obese subjects. In leptin resistance, your leptin level is high, which means you are high in fat. Your brain is unaware of this and thinks it is starving, while in reality your body is overweight. This is caused by the body not working properly and not returning to homeostasis.
The human body works to keep balance among its numerous internal parts so that all the processes they are responsible for function properly. Homeostasis is the state of internal equilibrium and it comes as a result of the proper functioning efforts of the body's organ systems. Though organs in the body play roles in maintaining homeostasis, hormones are extremely important in sustaining and regulating it.
Chapter 11 Hormones and Stress
A stressor is anything that interrupts the physiological balance in an organism. It can be physical or mental. As a reaction to stress, organisms respond in a physiological and behavioral manner to reestablish homeostasis. Many stressful events such as illness, injury, exams, etc. can lead to generalized stress responses from the body. The effects of stress are thought to be mediated by the activation of the HPA axis. Environmental challenges are part of the daily life of any person. As our society becomes more industrialized, stress seems to have increased. Essentially every piece of our body and brain can be affected. Though its effects are partly mediated by strong corticosteroid hormones that target the nervous system, relatively little is known about when, and how, the effects of stress shift from being beneficial and protective to becoming harmful.
Symptoms of a person who claims to be stressed are generally categorized by memory and focus problems, fatigue, irritability, and anxiety. The underlying pathophysiology of these problems has been described as a breakdown of the HPA axis, which normally helps to normalize stress. Studies have shown that the regulation of the HPA axis is mediated by three limbic structures: the hippocampus, the amygdala and the anterior prefrontal cortex. Persistent daily psychosocial stress seems to be associated with a limbic reduction of 5-HT1A receptor binding and functional disintegration of ACC/mPFC (Jovanic et al). In a study conducted by H. Jovanic et al, the notion of an impaired top-down regulation of stress stimuli, and identify potential targets for early treatment. Dysfunction of the limbic system can lead to psychopathologies such as depression and bi polar disorder. This study supports stress as a leading cause to human disease.
Posttraumatic stress disorder is an anxiety disorder that occurs worldwide. This disorder is known to be cause directly by stress, reasons why stress is in the name. Physiological stimulation during a stressful event can contribute to the development of this type of disorder. Administration of epinephrine to the peripheral immediately after extreme training increases the joining of amygdala-mediated learning in animals. Low cortisol levels in a rape victim have been found to be associated with a higher risk for developing PTSD. Low corticosterone levels may extend the adrenergic response to stress and enhance the effect of catecholamine’s on memory in animals (Shalev et al, 1998). Biological excitement during traumatic events may trigger the neurobiological processes that lead to posttraumatic stress disorder. Shalev et al ran a study that looked at the relationship between heart rate and blood pressure after a traumatic event and the subsequent development of PTSD. When blood pressure and heart rate is elevated and then measured shortly after trauma, it has been found to be associated with the later development of PTSD
Stress is thought to contribute to the differences of the aging process and to the development of age-related neuro- and psychopathologies (Solas et al, 2010). Glucocorticoid secretion, a steroid hormone, related with early life stress may contribute to the variability of the aging process and to the development of neuro-psychopathologies and psychopathologies. The effects of stress are thought to be culminating in increased levels of glucocorticoids by the activation of the HPA axis. Stress in aged rats and humans have shown an immense loss of HPA axis control which leads to hypersecretion of glucoticoids. This reaction is involved in age-related diseases such as depression and memory impairments. Results of a study conducted by Maite Solas et al, concluded that aging interactions with stress have an influence on cognition as the basis of Alzheimer disease. The study projects the idea for the use of glucocorticoid-/insulin-related drugs in the treatment of Alzheimer disease all due to stress.
The hippocampus is a target for glucocorticoid stress hormones, which stimulate hippocampal aging. Examples of the hippocampal aging are, decreased neuronal density, altered synaptic plasticity, dendritic atrophy, and spatial learning deficits (Jeong et al,2006). The hippocampus is a vulnerable region in Alzheimer’s disease. The experiment ran by Jeong at al studied the effect of stress on mice. The amounts of vascular and extracellular deposits holding amyloid beta peptide (Abeta) and carboxyl-terminal fragments of amyloid precursor protein (APP-CTFs), which are pathologic markers of Alzheimer’s disease, were considerably high in stressed mice, especially in the hippocampus area. Its findings were that chronic stress is an important pathogenic factor in the onset and development of AD.
Exposure to stress can cause many mental illnesses such as major depressive disorder and post-traumatic stress disorder. Irregular activity in the medial prefrontal cortex and amygdala is usually perceived in these disorders. Irregular activity can occur when medial prefrontal cortex activity is suppressed while the amygdala activity is increased (Shansky et al, 2009). The study conducted by Shansky et al, tested that neurons in the infralimbic region of the medial prefrontal cortex would endure morphological changes due to stress when projected to the basolateral nucleus of the amygdala. This was compared to randomly chosen neurons or neurons that project to other cortical areas in the brain. The study concluded that the areas in the brain appear to be mainly resistant against the effects of chronic stress. While most studies aim that stress can cause disease, this study has shown opposition to that claim.
The body's response to stress is usually for a short amount of time. Once the stressor has passed, the body returns to homeostasis. Adrenaline levels, cortisol levels, and blood pressure return to normal and other systems continue their regular activities. This does not always happen when a stressor does not go away. The continuous activation of the stress-response system and the ongoing exposure to cortisol and other stress hormones can interfere with almost all of the body's processes. Though some studies have proven that stress is not a leading cause of disease, this generally puts organisms at risk for health problems.
Chapter 13 – Hormones and Mood
Psychiatric diseases, called mood disorders are types of affective disorders. Depression, bipolar disorder, and anxiety disorder all affect moods and are the three main types of affective disorders. They can range from mild to severe. The cause of affective disorders can vary. Studies have shown that hormones and neurotransmitters can cause an imbalance that leads to affective disorders. Mood disorders tend to result in removing one’s self from social activity and difficulties at work. For many years the pathogenesis of affective disorders has been explored. Results have suggested genetic influence to the development of them. Hormonal imbalances caused by pathology and inherited predisposition can cause behavioral disorders and can result in psychological distress.
The presence of physical and psychological symptoms occurring during the late luteal phase of the menstrual cycle is premenstrual syndrome, familiarly known as PMS. PMS is associated with extensive loss in social relationships, lifestyle, and school performance. Ovarian hormones and neurotransmitters play a vital role in PMS. In a study conducted by Masoumi, Ataollahi, and Oshvandi, 2016, vitamins B6 and calcium deficiencies, and reduced serotonin levels were linked to the cause of the disorder, causing an imbalance within the bodily system. PMS may reflect a pathological state brought about by chronic fluctuations in hormone concentrations. Abrupt withdrawal from gonadal steroid hormones, due to an imbalance, may cause symptoms. The cause of PMS is continuously being studied to try and understand the physiological, behavioral and social causes
Serotonin receptors, also knows as 5-HT, are linked to affective disorders such as depression and bipolar. Over the last few years studies on affective disorders have mainly looked at genetic links such as serotonergic neurotransmitters and serotonin receptors (Anguelova, Benkelfat, and Turecki, 2003). Anorexia nervosa has a strong genetic link. Genes encoding for: 5-HTT are responsible for terminating 5-HT, serotonin receptors, neurotransmission. High doss treatment with SSRI’s on people with this genetic encoding can play a role in treating people with anorexia. Also, treatment that blocks MC4 – R may be effective as well on patients.
Changes in the HPA and HPT axes have shown to be important in neuroendocrine abnormalities in depression. A hyperactive HPA axis is one of the most well-known neuroendocrine abnormalities in depression. A hyperactive HPA axis can be a trait in changes that take place in monoaminergic pathways that moderate hormonal response. Dysfunction in the HPT axis is another common neuroendocrine abnormality in depression. The h 5-HT and the HPA axis relationship causes the failure to respond normally to DEX, the hypersecretion of cortisol, and disruption to the circadian rhythm of cortisol secretion. In the study conducted by Min et al, results indicated that the HPA axis was generally associated with many symptoms of depression due to abnormalities. A high amount of cortisol would cause impairments in the hippocampus and locus ceruleus which would lead to a memory, behavior, and attention dysfunctions. The findings in the study support that patients with HPA axis abnormalities possibly have affective disorders such as depression. In the same study in the HPT axis, thyroxine was linked to sever depression. Depressed patients with HPT dysfunction were vulnerable to multiple health issues such as sleep disorders, weight loss and stomach problems. This study mainly concludes associations between clinical manifestations of depression and the dysfunctions of HPA and HPT axes have a high correlation.
Postpartum depression is a type of depression that can affect women after they give birth to a child. Symptoms of postpartum can be sadness, fatigue, reduced sex drive, and irritability. Over the years there have been developing factors on what causes post-partum depression. A link has been found between placental corticotrophine-releasing hormone and post-partum depression. The Corticotropin-releasing hormone is a peptide hormone and neurotransmitter involved in the stress response. In Yim, eat al’s study they tested the relationship between pCRH and post-partum depression. Results indicated that during pregnancy, pCRH is a sensitive and specific early diagnostic test for PPD symptoms. The data indicated that pCRH is a possible diagnostic tool to identify women at risk for the development of PPD symptoms.
Besides humans, animals have been used in previous studies to test affective disorders. Schizophrenia has been tested in mice models in the study conducted by Y Ayhan, et al. Schizophrenia is a mood disorder that affects how a person thinks, acts, and feels. Genetic evidence associates mutations and polymorphisms with the gene Disrupted-In-Schizophrenia-1, thus resulting in the mood disorder schizophrenia or even a different type of disorder. This gene has been tested and results have shown that DISC1 is contingent on when neurodevelopment expression of the protein occurs. Across numerous stages, DISC1 has different functions across of neurodevelopment and adulthood. This can somewhat explain varied DISC1-associated pathological manifestations, such as schizophrenia and potentially provide a model for aspects of major mental diseases. (Y. Ayhan et al, 2011).
Many endocrine factors play vital roles in the development of affective disorders. With ongoing research, both on humans and animals, understanding how the neuroendocrinology system and affective disorders are related can help possibly diminish the progression of disorders.
Extra Credit
It was a Saturday night; there was a boxing match on TV, so my fiancé and I got together with some friends to watch the big fight. While the boys were wrapped up in the preliminaries, I sat and chatted with a girlfriend of mine. We were on the topic of pregnancy. A good friend of hers is having trouble getting pregnant. She could not remember what it was causing the trouble. She said to me “it’s not estrogen, it’s something else”. “Progesterone?” I asked. She said “that’s it!” And then my knowledge of progesterone from Behavioral Neuroendocrinology came spewing out. I never knew a thing about progesterone until I enrolled into the Psych 309 Behavioral neuroendocrinology course. Pretty sad considering it’s something I produce monthly. My friend also was not aware of its function or even that is existed!
Progesterone is an extremely vital female hormone and crucial to the female menstrual cycle. It preps the uterus for pregnancy, and keeps females menstrual cycle regulated. Each month a female ovulates, and progesterone helps thicken the uterus lining for an egg in case it is fertilized. The pituitary gland in the brain produces the hormones FSH and LH. Both these hormones cause a new egg to mature and be released from its ovarian follicle each month. As the follicle develops, it produces estrogen and progesterone. When estrogen reaches its peak, it causes the release of progesterone. The release of progesterone causes an LH surge which leads to a follicle rupture and the release of ovaries. With these events, the cavity of the ruptured follicle fills with blood and forms the corpus luteum. The cells of the corpus luteum produce estrogen and progesterone for the rest of the cycle. If there is no pregnancy, the corpus luteum begins to shed and progesterone levels decrease. If an egg is fertilized, progesterone levels will remain high. Some behaviors regulated by progesterone are: calms anxiety, promotes normal sleep patterns, helps normalize blood sugar, regulates sleep patterns and maintain libido.
When females fail to ovulate, the ovaries do not produce progesterone. This is called an anovulatory cycle. Women can begin to skip ovulations as early as their 30s. Missed ovulations that are frequent lead towards menopause. By postmenopause a woman's progesterone will drop to just about zero. In some cases, other than menopause, if progesterone is absent or too low, irregular and heavy bleeding can occur during menstruation. If a woman is pregnant and her progesterone levels drop it can result in a miscarriage and early labor. Lack of progesterone in the bloodstream can mean the ovary has failed to release an egg at ovulation, as can occur in women with polycystic ovary syndrome. There are fertility treatments for women with little to no levels of progesterone.
Progesterone can also be found in males. Progesterone in males helps to reverse the effect of estrogen. Progesterone turns into testosterone. Not only is progesterone found in males, but men rely on this hormone to preserve their masculinity. As estrogen levels increase in men, there is no similar rise in progesterone to balance this. For men, progesterone is therefore anti-feminizing.
The beginning scenario goes to show how ignorant women are of their own bodies, including myself! As a 27 year old female, getting married next year and eventually hoping to have children – I just learned what progesterone was and what is does. Parents and even schools should take into consideration the importance of females and males understanding what their bodies produce and do.
References
Ch 8
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Ch 9
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Ch 13
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